Affinage

WNT10B

Protein Wnt-10b · UniProt O00744

Length
389 aa
Mass
43.0 kDa
Annotated
2026-04-28
100 papers in source corpus 34 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

WNT10B is a secreted Wnt ligand that activates canonical β-catenin/TCF signaling to govern mesenchymal stem cell fate decisions, hair follicle cycling, midbrain-hindbrain boundary patterning, and mitotic fidelity. In bone and adipose tissue, WNT10B promotes osteoblastogenesis by inducing Runx2, Dlx5, and osterix while suppressing the adipogenic transcription factors C/EBPα and PPARγ, and Wnt10b-null mice exhibit progressive trabecular bone loss and increased adiposity (PMID:15728361, PMID:15190075, PMID:20499361); intermittent PTH drives bone anabolism specifically through CD8+ T-cell-produced WNT10B acting on preosteoblasts via an NFAT1–SMAD3-dependent transcriptional mechanism (PMID:19723499, PMID:30446387). WNT10B expression is regulated epigenetically by NSD1 (H3K36me2), MAT2A–EZH2 (H3K27me3), and BMI1 (H2AK119ub) at its locus, and post-transcriptionally by miR-148a targeting its 3′-UTR (PMID:31727171, PMID:29133280, PMID:35541907, PMID:22890324). Loss-of-function WNT10B mutations that abolish canonical signaling cause human oligodontia, and MMTV-driven overexpression in the mammary gland induces adenocarcinoma cooperatively with FGF signaling, while in triple-negative breast cancer WNT10B drives proliferation through a β-catenin–HMGA2–EZH2 transcriptional axis (PMID:27321946, PMID:9393971, PMID:23307470).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1997 High

    Whether WNT10B had oncogenic potential was unknown; transgenic mammary overexpression established it as a proto-oncogene that cooperates with FGF signaling to drive mammary adenocarcinoma.

    Evidence MMTV-Wnt10b transgenic mice and MMTV-Wnt10b × MMTV-FGF-3 crosses with tumor incidence analysis

    PMID:9393971

    Open questions at the time
    • Mechanism of FGF–WNT10B oncogenic cooperation undefined
    • Downstream intracellular signaling in mammary tumors uncharacterized at this stage
  2. 2003 High

    Whether wnt10b had roles in embryonic patterning was unknown; zebrafish studies showed that wnt1 and wnt10b function redundantly to maintain Pax2.1 expression at the midbrain-hindbrain boundary.

    Evidence Zebrafish wnt1-wnt10b deficiency allele with morpholino knockdown and genetic epistasis

    PMID:12591239

    Open questions at the time
    • Whether mammalian WNT10B has analogous brain patterning roles not established
    • Receptor identity for WNT10B in this context unknown
  3. 2005 High

    The physiological role of WNT10B in mesenchymal cell fate was unknown; gain- and loss-of-function mouse models demonstrated that WNT10B directs mesenchymal progenitors toward osteoblastogenesis (via Runx2/Dlx5/osterix) and away from adipogenesis (by suppressing C/EBPα/PPARγ) through canonical β-catenin signaling, and simultaneously suppresses adipose tissue development and prevents obesity.

    Evidence FABP4-Wnt10b transgenic mice, Wnt10b−/− knockout mice, body composition analysis, β-catenin manipulation, gene expression analysis

    PMID:15190075 PMID:15673614 PMID:15728361

    Open questions at the time
    • Whether WNT10B acts cell-autonomously versus paracrine in vivo not fully resolved
    • Frizzled receptor specificity not determined
  4. 2007 High

    Whether WNT10B acts solely through canonical Wnt signaling was unresolved; osteoblast-specific overexpression confirmed bone-anabolic effects through increased osteoblast number without affecting osteoclasts, while parallel work revealed β-catenin-independent growth-suppressive activity that could be switched by FGF signaling.

    Evidence Osteocalcin-Wnt10b transgenic and Wnt10b−/− mice with histomorphometry; dominant-negative TCF-4 and β-catenin mutant transduction in cancer cells

    PMID:17708715 PMID:17761539

    Open questions at the time
    • Identity of β-catenin-independent signaling effector unknown
    • Mechanism by which FGF switches WNT10B from suppressor to promoter not resolved
  5. 2009 High

    The cellular source of WNT10B in PTH-driven bone anabolism was unknown; T-cell-specific Wnt10b deletion demonstrated that CD8+ T cells are the essential paracrine source of WNT10B mediating intermittent PTH's osteogenic effects.

    Evidence T-cell-null mice, T-cell-specific Wnt10b conditional knockout, iPTH treatment with bone histomorphometry

    PMID:19723499

    Open questions at the time
    • Mechanism by which PTH signals to CD8+ T cells to induce Wnt10b expression not yet identified
    • Whether other immune cells contribute WNT10B in different contexts unclear
  6. 2011 High

    Whether WNT10B activates non-canonical pathways was systematically addressed; WNT10B was shown to activate NF-κB and Notch signaling in addition to canonical Wnt, and its anti-adipogenic/pro-osteogenic functions were confirmed to be entirely β-catenin-dependent by epistasis experiments.

    Evidence β-catenin knockdown in ST2 cells abolishing differentiation effects; NF-κB and Notch reporter assays in U2OS cells

    PMID:21321991 PMID:21872687

    Open questions at the time
    • Whether NF-κB/Notch activation by WNT10B is direct or indirect not established
    • NF-κB/Notch activation observed in single cell line only
  7. 2012 High

    Post-transcriptional regulation of WNT10B was unknown; miR-148a was identified as a direct negative regulator targeting the WNT10B 3′-UTR, and WNT10B was shown to drive hair follicle telogen-to-anagen transition through β-catenin signaling.

    Evidence 3′-UTR luciferase reporter and conditioned medium migration assays; adenoviral Wnt10b with β-catenin siRNA in mouse skin

    PMID:22832493 PMID:22890324

    Open questions at the time
    • Whether miR-148a is the dominant post-transcriptional regulator of WNT10B in vivo not established
    • Upstream signals activating Wnt10b in hair follicle stem cells not determined
  8. 2013 High

    Multiple transcriptional and paracrine regulatory inputs to WNT10B were identified: HIF-2α directly binds the Wnt10b enhancer under hypoxia, XBP1 directly represses the Wnt10b promoter during adipogenesis, TGF-β1 induces Wnt10b in osteoclasts via Smad2/3 for coupling to osteoblast mineralization, and WNT10B drives TNBC proliferation through a β-catenin–HMGA2–EZH2 transcriptional axis.

    Evidence ChIP for HIF-2α and XBP1 at Wnt10b regulatory regions; Smad2/3 inhibition with DKK1 blockade; ChIP plus Hmga2 haploinsufficiency in MMTV-Wnt10b tumors

    PMID:23307470 PMID:23603388 PMID:23861379 PMID:23900840

    Open questions at the time
    • Whether HIF-2α regulation of Wnt10b operates in bone cells not tested
    • Relative contributions of XBP1 direct repression versus XBP1s→miR-148a indirect repression not quantified
  9. 2013 High

    The role of WNT10B in hematopoietic progenitor regulation was unknown; estrogen deficiency was shown to expand short-term HSPCs through a CD40L→T-cell WNT10B pathway, demonstrating WNT10B as a niche signal linking immune and hematopoietic compartments.

    Evidence CD40L-null, global and T-cell-specific Wnt10b−/− mice with HSPC flow cytometry after ovariectomy

    PMID:23954891

    Open questions at the time
    • Whether WNT10B acts directly on HSPCs or through intermediate niche cells unclear
    • Frizzled receptor on HSPCs not identified
  10. 2016 High

    The XBP1s→miR-148a→Wnt10b axis was mechanistically resolved by demonstrating that XBP1s directly transactivates miR-148a, which then silences Wnt10b during adipogenesis; concurrently, human WNT10B loss-of-function mutations were shown to cause oligodontia by abolishing canonical signaling required for tooth development.

    Evidence ChIP for XBP1s at miR-148a promoter with point mutation validation; TOPFlash assays with naturally occurring human WNT10B mutants in dental pulp stem cells

    PMID:27055562 PMID:27321946

    Open questions at the time
    • Whether XBP1s→miR-148a axis operates in tissues beyond adipocytes not addressed
    • Full spectrum of WNT10B-associated dental phenotypes not delineated
  11. 2017 High

    Novel delivery and signaling modes for WNT10B were discovered: fibroblast-derived exosomes mobilize autocrine WNT10B to lipid rafts activating mTOR via GSK3β/TSC2 for CNS axon regeneration, paracrine exosomal WNT10B promotes breast cancer EMT, and MAT2A–EZH2 epigenetically represses Wnt10b via H3K27me3 during adipogenesis.

    Evidence Wnt10b−/− mice with optic nerve crush; p85α-knockdown fibroblast exosomes in co-culture; ChIP for MAT2A and H3K27me3 at Wnt10b promoter with enzyme inhibition

    PMID:28394344 PMID:28683327 PMID:29133280

    Open questions at the time
    • Whether exosomal versus free WNT10B have different receptor engagement not resolved
    • Structural basis for WNT10B sorting into exosomes unknown
  12. 2018 High

    The upstream transcriptional mechanism driving T-cell Wnt10b expression was identified: Treg cells promote assembly of an NFAT1–SMAD3 complex in CD8+ T cells that drives Wnt10b transcription, linking the gut microbiome (butyrate/Treg expansion) to bone anabolism via WNT10B.

    Evidence Germ-free mice, LGG/butyrate supplementation, reconstitution with Wnt10b−/− CD8+ T cells, Treg depletion, transcription factor complex analysis

    PMID:30446387

    Open questions at the time
    • Whether NFAT1–SMAD3 directly binds the Wnt10b promoter not confirmed by ChIP
    • Whether other microbial metabolites feed into this axis unknown
  13. 2020 High

    A mitotic function for WNT10B was previously unrecognized; WNT10B was identified as the specific Wnt ligand required for autocrine LRP6-mediated GSK3β inhibition that ensures proper mitotic microtubule dynamics and faithful chromosome segregation (the Wnt/STOP pathway).

    Evidence LRP6 and Wnt10b knockdown in human somatic cells with quantitative microtubule dynamics and chromosome segregation analysis

    PMID:33257473

    Open questions at the time
    • Whether WNT10B/STOP function is conserved across cell types not broadly tested
    • Identity of the GSK3β substrates mediating microtubule stabilization in mitosis not determined
  14. 2022 High

    Epigenetic repression of Wnt10b by BMI1 was established in spermatogonial stem cells, where BMI1 deposits H2AK119ub and reduces H3K4me3 at the Wnt10b locus to keep canonical Wnt signaling low, which is essential for SSC self-renewal.

    Evidence BMI1 knockout mice, ChIP for H2AK119ub and H3K4me3 at Wnt10b, Wnt/β-catenin inhibitor rescue

    PMID:35541907

    Open questions at the time
    • Whether BMI1 directly binds the Wnt10b locus or acts indirectly not shown
    • Whether WNT10B is the sole PRC1 target mediating the SSC phenotype not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The Frizzled receptor(s) and co-receptors mediating WNT10B's tissue-specific signaling outcomes remain unidentified, and the structural basis for how WNT10B engages canonical versus non-canonical (NF-κB, Notch, RAC1) pathways is unresolved.
  • No receptor-binding or structural data for WNT10B
  • Mechanism distinguishing canonical from non-canonical WNT10B signaling unknown
  • Whether WNT10B lipid modifications affect receptor selectivity not studied

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 6 GO:0098772 molecular function regulator activity 4
Localization
GO:0005576 extracellular region 4 GO:0031410 cytoplasmic vesicle 2 GO:0005886 plasma membrane 1 GO:0005929 cilium 1
Pathway
R-HSA-162582 Signal Transduction 8 R-HSA-1266738 Developmental Biology 4 R-HSA-1643685 Disease 3 R-HSA-1640170 Cell Cycle 1
Partners
CTNNB1EZH2GSK3BHMGA2LRP6RAC1

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 Wnt10b shifts mesenchymal precursor cell fate toward the osteoblast lineage by inducing osteoblastogenic transcription factors Runx2, Dlx5, and osterix, and suppressing adipogenic transcription factors C/EBPα and PPARγ, acting through canonical Wnt/β-catenin signaling. Wnt10b-/- mice have decreased trabecular bone and serum osteocalcin, confirming its endogenous role in bone formation. Transgenic mouse overexpression (FABP4-Wnt10b), Wnt10b-/- knockout mice, pharmacological and genetic approaches (β-catenin manipulation), gene expression analysis Proceedings of the National Academy of Sciences of the United States of America High 15728361
2004 Wnt10b inhibits development of both white and brown adipose tissue in vivo; transgenic expression from the FABP4 promoter blocks adipogenesis throughout the body, reduces total body fat ~50%, and prevents diet-induced obesity, demonstrating Wnt10b is a physiological regulator of adipogenesis. FABP4-Wnt10b transgenic mice, body composition analysis, histology, metabolic measurements The Journal of biological chemistry High 15190075
2011 Wnt10b (and Wnt6 and Wnt10a) inhibit adipogenesis and stimulate osteoblastogenesis exclusively through a β-catenin-dependent mechanism; knockdown of β-catenin completely abolishes these effects of all three Wnt ligands in bipotential ST2 mesenchymal cells. Gain- and loss-of-function in ST2 and 3T3-L1 cells, β-catenin knockdown, differentiation assays Bone High 21872687
2009 Intermittent PTH increases Wnt10b production by bone marrow CD8+ T cells, which then activates canonical Wnt signaling in preosteoblasts to stimulate osteoblastic commitment, proliferation, differentiation, and life span; T-cell-null mice and mice lacking T-cell-produced Wnt10b show no anabolic response to iPTH. T cell-null mice, conditional Wnt10b knockout (T-cell-specific), iPTH treatment, bone histomorphometry, Wnt reporter assays Cell metabolism High 19723499
2005 In myoblasts, Wnt10b deficiency increases adipogenic potential and promotes coexpression of myogenic and adipogenic programs; decreased Wnt10b in aged myoblasts contributes to excessive lipid accumulation. Mimicking Wnt signaling via Wnt10b overexpression or GSK3 inhibition restores myogenic differentiation and suppresses adipogenic gene expression. Wnt10b-/- mice, overexpression in aged myoblasts, GSK-3 inhibition, in vitro differentiation assays, in vivo muscle regeneration Molecular biology of the cell High 15673614
1997 Overexpression of Wnt10b in the mouse mammary gland via MMTV promoter causes hypermorphic mammary gland development (precocious alveologenesis, ductal branching in males) and high susceptibility to mammary adenocarcinoma; co-expression with FGF-3/int-2 causes a potent synergistic interaction, indicating Wnt10b is a proto-oncogene that cooperates with FGF signaling. MMTV-Wnt10b transgenic mice, MMTV-Wnt10b × MMTV-FGF-3 crosses, histology, tumor incidence Oncogene High 9393971
2007 Osteoblast-specific overexpression of Wnt10b (from osteocalcin promoter) increases bone mass primarily by stimulating osteoblastogenesis, specifically increasing osteoblast number per bone surface, mineral apposition rate, and mineralizing surface, without altering pre-osteoblast proliferation, osteoblast apoptosis, or osteoclast number; Wnt10b-/- mice show reduced bone formation rate. Oc-Wnt10b transgenic mice, Wnt10b-/- mice, μCT, histomorphometry, BrdU, TUNEL, TRACP5b assays Journal of bone and mineral research High 17708715
2010 Wnt10b is required for maintenance of adult bone density and mesenchymal progenitor cells (MPCs); Wnt10b-null mice show progressive age-dependent loss of trabecular bone associated with reduction in bone marrow-derived MPC number and decreased osteoblast differentiation marker expression. Wnt10b-null mice, μCT, bone histomorphometry, colony-forming unit assays, osteogenic gene expression in primary BMSCs Journal of bone and mineral research High 20499361
2013 WNT10B activates canonical β-catenin signaling leading to transcriptional upregulation of HMGA2 in triple-negative breast cancer (TNBC); HMGA2 is necessary and sufficient for WNT10B-driven proliferation; HMGA2 and EZH2 displace Groucho/TLE1 from TCF-4 and mediate K49 acetylation on β-CATENIN required for transcription. ChIP analysis, siRNA knockdown, WNT/β-catenin pathway modulators, MMTV-Wnt10b transgenic tumors, luciferase reporter, Hmga2 haploinsufficiency mouse model EMBO molecular medicine High 23307470
2018 Butyrate-induced expansion of regulatory T (Treg) cells promotes Treg-CD8+ T cell interaction, leading to increased Wnt10b secretion by CD8+ T cells; mechanistically, Treg cells drive assembly of a NFAT1-SMAD3 transcription complex in CD8+ T cells, which drives Wnt10b expression and bone anabolism. Germ-free mouse models, LGG probiotic/butyrate supplementation, TCRβ-/- reconstitution with Wnt10b-/- CD8+ T cells, Treg cell depletion, transcription factor complex analysis Immunity High 30446387
2012 miR-148a directly targets the 3'-UTR of WNT10B mRNA in cancer-associated fibroblasts; silencing of miR-148a in CAFs increases WNT10B protein levels and stimulates migration of endometrial cancer cells through Wnt/β-catenin pathway activation. 3'-UTR luciferase reporter assay, lentiviral miR-148a overexpression, conditioned medium migration assays, SuperTOPFlash reporter Oncogene High 22890324
2013 TGF-β1 stimulates Wnt10b production in osteoclasts through Smad2/3 activation (independent of AKT or MAPK), which then promotes osteoblast mineralization; blocking Wnt10b activity with DKK1 suppresses TGF-β-treated osteoclast-conditioned medium-induced mineralization. Osteoclast-conditioned medium, DKK1 inhibition, Smad2/3 signaling blockade, mineralization assays Endocrinology High 23861379
2014 The Scl-independent bone anabolic activity of intermittent PTH is mediated specifically by T-cell-produced Wnt10b; combined Scl-Ab and iPTH treatment is equally effective as Scl-Ab alone in T-cell-null and T-cell-specific Wnt10b-knockout mice, demonstrating epistatic relationship. T-cell-null mice, T-cell-specific Wnt10b-/- mice, anti-sclerostin antibody, iPTH treatment, bone densitometry, histomorphometry Journal of bone and mineral research High 24357520
2017 Fibroblast-derived exosomes (FD exosomes) mobilize autocrine Wnt10b toward lipid rafts, activating the mTOR pathway via GSK3β and TSC2; Wnt10b-deleted animals show strongly reduced axonal regeneration after optic nerve injury in response to FD exosomes, establishing an autocrine Wnt10b-mTOR pathway for CNS axonal regeneration. Wnt10b-deleted mice, FD exosome application, optic nerve crush model, lipid raft fractionation, mTOR/GSK3β/TSC2 pathway analysis Cell reports High 28683327
2006 A naturally occurring missense mutation C256Y in WNT10B abrogates the ability of WNT10B to activate canonical Wnt signaling and block adipogenesis, establishing that WNT10B canonical signaling activity is required for its anti-adipogenic function in humans. Functional assay of canonical Wnt signaling activity and adipogenesis inhibition for naturally occurring human WNT10B missense variants Diabetologia High 16477437
2012 Wnt10b overexpression induces hair follicle regeneration by switching follicles from telogen to anagen via canonical Wnt signaling; β-catenin translocates to the nucleus in Wnt10b-induced follicles; knockdown of β-catenin abrogates Wnt10b's biological effects on hair follicle cycling. Adenovirus-mediated Wnt10b overexpression, siRNA knockdown of Wnt10b and β-catenin, in vivo mouse intradermal injection model, histology The Journal of investigative dermatology High 22832493
2011 Wnt10b activates canonical Wnt, NFκB, and Notch signaling pathways in U2OS osteosarcoma cells; Wnt3a fails to induce NFκB and Notch activation, demonstrating Wnt10b-specific activity beyond canonical Wnt/β-catenin signaling. Stable Wnt10b-expressing U2OS cell line, microarray, NFκB and Notch reporter assays, gene expression analysis Journal of cellular biochemistry Medium 21321991
2015 WNT10B promotes proliferation of human corneal endothelial cells through simultaneous β-catenin-dependent and β-catenin-independent pathways; specifically, WNT10B causes nuclear transport and binding of both RAC1 and β-catenin, leading to Cyclin D1 expression. Wnt10b overexpression in human corneal endothelial cells, nuclear fractionation, RAC1 and β-catenin co-localization, Cyclin D1 reporter, proliferation assay The Journal of biological chemistry Medium 26370090
2013 Ovariectomy-induced estrogen deficiency expands short-term hematopoietic stem and progenitor cells (ST-HSPCs) through T-cell expression of CD40L, which stimulates T-cell production of Wnt10b; Wnt10b then activates Wnt signaling in HSPCs. Ovariectomy fails to expand ST-HSPCs in CD40L-null mice and in animals lacking global or T-cell expression of Wnt10b. CD40L-null mice, global and T-cell-specific Wnt10b-/- mice, bone marrow transplantation, HSPC flow cytometry Blood High 23954891
2016 XBP1s directly induces transcription of microRNA-148a, which in turn binds the 3'-UTR of Wnt10b mRNA and mediates silencing of Wnt10b during adipogenic differentiation of 3T3-L1 cells, establishing an XBP1s→miR-148a→Wnt10b regulatory axis. XBP1s knockdown/overexpression, miR-148a 3'-UTR reporter assay, ChIP for XBP1s at miR-148a promoter, point mutation analysis, mRNA stability assays Experimental & molecular medicine High 27055562
2013 XBP1 directly binds to the Wnt10b promoter and suppresses Wnt10b expression during 3T3-L1 preadipocyte differentiation, leading to decreased β-catenin signaling; XBP1 and Wnt10b show reciprocal expression patterns during early adipogenesis. XBP1 overexpression/knockdown, ChIP for XBP1 at Wnt10b promoter, β-catenin activity assays, expression profiling during adipogenesis FEBS letters Medium 23603388
2013 Hypoxia-inducible factor-2α (HIF-2α), but not HIF-1α, directly binds the Wnt10b enhancer region and drives Wnt10b expression under hypoxia in adipogenic cells; HIF-2α-deficient adipogenic cells fail to upregulate Wnt10b under hypoxia, and hypoxia-conditioned medium inhibits adipogenesis through canonical Wnt signaling. ChIP for HIF-2α at Wnt10b enhancer, HIF-2α-deficient adipogenic cells, hypoxia-conditioned medium experiments, β-catenin reporter assays The Journal of biological chemistry High 23900840
2019 NSD1 histone methyltransferase activates Wnt10b expression by mediating H3K36me2 methylation at the Wnt10b locus; NSD1 knockout promotes H3K27me3 and reduces H3K36me2 at the Wnt10b gene, suppressing its expression and thereby inactivating the Wnt/β-catenin pathway in HCC cells. CRISPR/Cas9 NSD1 knockout, ChIP for H3K27me3 and H3K36me2 at Wnt10b, proliferation/invasion assays, xenograft model Journal of experimental & clinical cancer research High 31727171
2017 MAT2A interacts with EZH2 and MafK, is recruited to the Wnt10b promoter, and represses Wnt10b expression by promoting H3K27 methylation; this Wnt10b suppression inhibits Wnt/β-catenin signaling to promote adipogenesis. MAT2A catalytic activity and its interaction with MAT2B are required for Wnt10b repression. ChIP for MAT2A and H3K27me3 at Wnt10b promoter, co-IP for MAT2A/EZH2/MafK interaction, MAT2A overexpression/knockdown, MATII enzyme inhibition Biochimica et biophysica acta. Molecular and cell biology of lipids High 29133280
2020 Wnt10b-GSK3β-driven autocrine canonical Wnt/LRP6 signaling is required for proper mitotic microtubule dynamics and faithful chromosome segregation in human somatic cells; inhibition of LRP6 signaling causes increased GSK3β activity, abnormal microtubule growth rates in mitotic spindles, and aneuploidy; Wnt10b is the specific Wnt ligand required for this Wnt/STOP function. LRP6/Wnt10b inhibition, microtubule dynamics measurement in mitosis, chromosome segregation analysis, Wnt10b knockdown in human somatic cells Life science alliance High 33257473
2021 PTEN reduces BMP9-induced osteogenic differentiation by decreasing Wnt10b expression; BMP9 signals through PI3K/CREB and Smad1/5/9, whose interaction drives Wnt10b transcription; p-CREB and p-Smad1/5/9 are both enriched at the Wnt10b promoter; PTEN disrupts this CREB-BMP/Smad interaction, reducing Wnt10b and osteogenesis. ChIP for p-CREB and p-Smad1/5/9 at Wnt10b promoter, co-IP for CREB/Smad interaction, PI3K inhibitor, rapamycin, PTEN and Wnt10b knockdown, MSC osteogenic assays, xenograft bone formation Frontiers in cell and developmental biology High 33614622
2017 Low expression of p85α in stromal fibroblasts leads to paracrine WNT10B transport via exosomes to breast cancer epithelial cells, promoting cancer progression through epithelial-to-mesenchymal transition (EMT) via the canonical Wnt pathway. p85α knockdown in fibroblasts, exosome isolation and characterization, co-culture systems, EMT marker analysis, canonical Wnt pathway reporter Oncogene Medium 28394344
2015 Wnt10b gain-of-function in cardiomyocytes after myocardial infarction stimulates VEGFR2 expression in endothelial cells and angiopoietin-1 in vascular smooth muscle cells through NF-κB activation, coordinating arteriole formation and reducing fibrosis. Wnt10b gain-of-function mouse line, coronary artery ligation/cryoinjury models, NF-κB activation assay, VEGFR2/angiopoietin-1 expression analysis, histology Circulation research Medium 26338900
2016 WNT10B mutations associated with oligodontia (e.g., R211Q, P190R, W262*, F284C) cannot normally enhance canonical Wnt signaling in TOPFlash reporter assays and cannot efficiently induce endothelial differentiation of dental pulp stem cells, establishing that WNT10B canonical signaling is required for tooth development. TOPFlash luciferase reporter assay for canonical Wnt signaling, endothelial differentiation assay of dental pulp stem cells with mutant WNT10B ligands, Sanger sequencing, whole-exome sequencing American journal of human genetics Medium 27321946
2022 BMI1 epigenetically represses Wnt10b expression in spermatogonial stem cells (SSCs) by increasing H2AK119ub and reducing H3K4me3 at the Wnt10b locus; BMI1 inhibition causes transcriptional activation of Wnt10b and nuclear translocation of β-catenin, impairing SSC maintenance; suppression of Wnt/β-catenin signaling rescues SSC maintenance in BMI1-deficient SSCs. BMI1 knockout mouse model, ChIP for H2AK119ub and H3K4me3 at Wnt10b locus, β-catenin localization, Wnt/β-catenin inhibitor rescue experiments International journal of biological sciences High 35541907
2007 WNT10B exhibits a functional dualism: it up-regulates β-catenin/Tcf activity (canonical Wnt signaling), but also independently suppresses cell growth and anchorage-independent growth through a β-catenin/Tcf-independent mechanism; FGF signaling switches WNT10B from growth suppressor to growth promoter. WNT10B promoter is aberrantly methylated and silenced in 46% of primary HCC. β-catenin/Tcf reporter assay, dominant-negative TCF-4, β-catenin mutant transduction, growth assays, 5-aza-2'deoxycytidine reactivation, FGF co-treatment Molecular biology of the cell Medium 17761539
2011 Leucine-rich amelogenin peptide (LRAP) promotes osteogenesis over adipogenesis in mesenchymal stem cells through upregulation of Wnt10b expression; Wnt10b knockdown by siRNA abrogates the osteogenic effect of LRAP, and a Wnt inhibitor (sFRP-1) abolishes LRAP's effects, placing Wnt10b downstream of LRAP in the canonical Wnt signaling pathway. ST2 cell overexpression and Wnt10b siRNA knockdown, sFRP-1 treatment, osteogenesis and adipogenesis assays Biomaterials Medium 21663957
2019 Sinusoidal electromagnetic fields promote osteogenic differentiation of osteoblasts through activation of the Wnt10b/β-catenin pathway in a manner dependent on the functional integrity of primary cilia; Wnt10b is localized at the base of primary cilia and is released upon SEMF treatment; siRNA knockdown of IFT88 (abrogating primary cilia) blocks SEMF-induced Wnt10b/β-catenin activation. siRNA knockdown of IFT88 and Wnt10b, immunofluorescence for primary cilia and Wnt10b localization, osteogenic differentiation assays, in vivo rat model with μCT Journal of bone and mineral research Medium 30779853
2003 In zebrafish, wnt1 and wnt10b function redundantly to maintain threshold levels of Pax2.1 and Fgf8 at the midbrain-hindbrain boundary (MHB); double deletion of both loci causes loss of pax2.1, en2, and her5 expression in the ventral MHB without affecting fgf8, en3, wnt8b, or wnt3a. Zebrafish wnt1-wnt10b deficiency allele, morpholino antisense knockdown, in situ hybridization, genetic epistasis with pax2.1 and fgf8 mutants Developmental biology High 12591239

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Regulation of osteoblastogenesis and bone mass by Wnt10b. Proceedings of the National Academy of Sciences of the United States of America 716 15728361
2018 The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. Immunity 409 30446387
2011 Wnt6, Wnt10a and Wnt10b inhibit adipogenesis and stimulate osteoblastogenesis through a β-catenin-dependent mechanism. Bone 355 21872687
2004 Wnt10b inhibits development of white and brown adipose tissues. The Journal of biological chemistry 296 15190075
2007 Wnt10b increases postnatal bone formation by enhancing osteoblast differentiation. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 229 17708715
2013 WNT10B/β-catenin signalling induces HMGA2 and proliferation in metastatic triple-negative breast cancer. EMBO molecular medicine 152 23307470
2010 Wnt10b deficiency results in age-dependent loss of bone mass and progressive reduction of mesenchymal progenitor cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 150 20499361
2007 Wnt10b inhibits obesity in ob/ob and agouti mice. Diabetes 143 17259372
2009 T lymphocytes amplify the anabolic activity of parathyroid hormone through Wnt10b signaling. Cell metabolism 142 19723499
2005 Wnt10b deficiency promotes coexpression of myogenic and adipogenic programs in myoblasts. Molecular biology of the cell 131 15673614
1997 Wnt-10b directs hypermorphic development and transformation in mammary glands of male and female mice. Oncogene 128 9393971
1995 Murine Wnt-11 and Wnt-12 have temporally and spatially restricted expression patterns during embryonic development. Mechanisms of development 123 7547479
2015 Loss of Bone and Wnt10b Expression in Male Type 1 Diabetic Mice Is Blocked by the Probiotic Lactobacillus reuteri. Endocrinology 117 26135835
2004 Identification of the mammary line in mouse by Wnt10b expression. Developmental dynamics : an official publication of the American Association of Anatomists 113 14745960
2012 Silencing of miR-148a in cancer-associated fibroblasts results in WNT10B-mediated stimulation of tumor cell motility. Oncogene 107 22890324
2006 WNT10B mutations in human obesity. Diabetologia 107 16477437
2017 Aberrant low expression of p85α in stromal fibroblasts promotes breast cancer cell metastasis through exosome-mediated paracrine Wnt10b. Oncogene 105 28394344
2009 Activation of Wnt/beta-catenin signaling increases insulin sensitivity through a reciprocal regulation of Wnt10b and SREBP-1c in skeletal muscle cells. PloS one 101 20041157
2012 Adenovirus-mediated Wnt10b overexpression induces hair follicle regeneration. The Journal of investigative dermatology 86 22832493
1996 Murine Wnt10a and Wnt10b: cloning and expression in developing limbs, face and skin of embryos and in adults. Oncogene 86 8875992
2017 Exosomes Mediate Mobilization of Autocrine Wnt10b to Promote Axonal Regeneration in the Injured CNS. Cell reports 85 28683327
2011 The role of WNT10B in physiology and disease. Acta physiologica (Oxford, England) 83 21447090
2016 Mutations in WNT10B Are Identified in Individuals with Oligodontia. American journal of human genetics 80 27321946
2003 Wnt1 and wnt10b function redundantly at the zebrafish midbrain-hindbrain boundary. Developmental biology 76 12591239
1997 A novel human Wnt gene, WNT10B, maps to 12q13 and is expressed in human breast carcinomas. Oncogene 74 9121776
2001 Proto-oncogene WNT10B is up-regulated by tumor necrosis factor alpha in human gastric cancer cell line MKN45. International journal of oncology 72 11713588
2011 Wnt10b promotes growth of hair follicles via a canonical Wnt signalling pathway. Clinical and experimental dermatology 67 21392083
2008 Homozygous WNT10b mutation and complex inheritance in Split-Hand/Foot Malformation. Human molecular genetics 65 18515319
2013 TGF-β induces Wnt10b in osteoclasts from female mice to enhance coupling to osteoblasts. Endocrinology 64 23861379
2018 MiR-148a suppressed cell invasion and migration via targeting WNT10b and modulating β-catenin signaling in cisplatin-resistant colorectal cancer cells. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 63 30551544
2014 Modulating hair follicle size with Wnt10b/DKK1 during hair regeneration. Experimental dermatology 61 24750467
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2008 Wnt10b induces chemotaxis of osteosarcoma and correlates with reduced survival. Pediatric blood & cancer 58 18465804
2014 The sclerostin-independent bone anabolic activity of intermittent PTH treatment is mediated by T-cell-produced Wnt10b. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 57 24357520
2004 Immunolocalization of BMP-2/-4, FGF-4, and WNT10b in the developing mouse first lower molar. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 55 14688221
2019 Coactivation of Endogenous Wnt10b and Foxc2 by CRISPR Activation Enhances BMSC Osteogenesis and Promotes Calvarial Bone Regeneration. Molecular therapy : the journal of the American Society of Gene Therapy 54 31882321
2015 Wnt10b Gain-of-Function Improves Cardiac Repair by Arteriole Formation and Attenuation of Fibrosis. Circulation research 52 26338900
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2020 Wnt10b-overexpressing umbilical cord mesenchymal stem cells promote critical size rat calvarial defect healing by enhanced osteogenesis and VEGF-mediated angiogenesis. Journal of orthopaedic translation 37 32477867
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2010 Homozygous nonsense mutation in WNT10B and sporadic split-hand/foot malformation (SHFM) with autosomal recessive inheritance. American journal of medical genetics. Part A 35 20635353
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2007 Ectopic expression of Wnt10b decreases adiposity and improves glucose homeostasis in obese rats. American journal of physiology. Endocrinology and metabolism 34 17578883
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